@article {10.3844/ajisp.2020.19.26, article_type = {journal}, title = {Blood-Circulating Type 2 Follicular Helper T Cells in Pediatric Allergy Patients}, author = {Hamada, Masaaki and Sakurai, Yoshihiko and Takeda, Tomohiro}, volume = {16}, year = {2020}, month = {Jun}, pages = {19-26}, doi = {10.3844/ajisp.2020.19.26}, url = {https://thescipub.com/abstract/ajisp.2020.19.26}, abstract = {Pediatric allergic diseases are primarily caused by an IgE-dependent immunological reaction. Despite studies reporting the involvement of T follicular Helper (TfH) cells, especially type 2 TfH cells, in class-switching to IgE production in B cells, TfH subset skewing in peripheral blood in pediatric allergy patients remains to be elucidated. This study aimed to investigate the possible involvement of type 2 TfH cells in the pathogenic mechanism underlying pediatric allergic diseases. We analyzed TfH subsets (type 1, type 2 and type 17) in peripheral blood from pediatric patients with (allergy group, 35 patients) and without (non-allergy group, 26 individuals) allergic diseases via flow cytometry to determine the percentage of each TfH subset in the total TfH cell repertoire. Furthermore, the eosinophil percentage and serum total IgE and Thymus and Activation-Regulated Chemokine (TARC) levels were measured. No significant differences were observed in sex and age between the allergy and non-allergy groups. Since IgE levels were significantly higher in the allergy group than in the non-allergy group, no significant overlap was observed in the number of patients in the allergy and non-allergy groups. Although the total IgE and TARC levels and the eosinophil percentage were significantly higher in the allergy group than in the non-allergy group, the TfH subset analysis did not display a significant skewing of specific TfH subset cells. These results suggest the occurrence of either limited changes in peripheral blood TfH cells or the involvement of the immune cell subtype TfH13 in pediatric allergic diseases.}, journal = {American Journal of Immunology}, publisher = {Science Publications} }